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Dept. of General Medicine VCSG Govt. Institute of Medical Science and Research

Gullian barre syndrome

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Nitin
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30 views14 pages

Dept. of General Medicine VCSG Govt. Institute of Medical Science and Research

Gullian barre syndrome

Uploaded by

Nitin
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© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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GUILLAIN BARRE

SYNDROME

Dept. of General Medicine


VCSG Govt. institute of
medical science and
research
GBS is a
polyradiculpneuropathy ,acute nd
frequently severe and autoimmune in
nature.

Males are at a higher risk than


females

In Western countries adults are


at a greater risk than children
PATHOPHYSIOLOGY AND
IMMUNOPATHOGENESIS
In demyelinating forms - flaccid paralysis and sensory
disturbance is due to conduction block ,hence
recovery occurs once remyelination takes place.
In severe cases axonal degeneration can occur ,
recovery is slower in such cases.

AIDP(ACUTE INFLAMMATORY
DEMUELINATING POLYNEUROPATHY)
Most studied form of GBS in which both cellular and
humoral immune response are responsible for tissue
damage .
All GBS results from immune response to non self
antigens(infectious agents , vaccines) that misdirect to
host nerve tissue i.e., molecular mimicry

The neural target is mainly glycoconjugates


(gangliosides) that are present largely in human
nervous system mainly at node of ranvier.

Antiganglioside antibody (mainly against GM1 ) is


common in GBS(20-50%) , particularly in AMAN(Acute
motor axonal neuropathy) and AMSAN(Acute motor
sensory axonal neuropathy) in which it is preceded
by C. JEJUNI infection.
Sialic acid residues from pathogenic strains of C.
jejuni can trigger dendritic cells via TLR4 promoting B
cell differentiation and amplifying humoral
autoimmunity

Anti GQ1b IgG antibodies are found in more than 90%


of patients with MFS(MILLER FISHER SYNDROME) and
titres are highest earlier in the course.

All these evidences suggest that autoantibodies


plys an important role in pathogenesis of GBS.
CLINICAL MANIFESTATION
Manifests as rapidly evolving areflexic motor
paralysis with or without sensory disturbance.

The usual pattern is ascending paralysis.

Weakness evolves over hours to few days.

Legs are more effected than arms and facial dipresis is


present in 50% of effected indivisuals.

Pain in neck,back,shoulders or diffusely over the


spine is also common in ealy stages of GBS , seen in
50% of indivisuals.
The need for mechanical ventilation is seen in cases
with more severe weakness on admission and facial
and/or bulbar weakness in first week of symptoms.

DTRs attenuate or disappear within first few days


of onset .

Autonomic involvement is common : Loss of


vasomotor control with wide fluctuations in BP ,
postural hypotension and cardiac dysrhyhtmias .
ANTECEDENT EVENTS

About 70% cases of GBS occurs after an acute


infective process , usually respiratory or
gastrointestinal.

Organisms like C. jejuni, viruses like HHV , CMV ,EBV ,


HIV , HEP E, and Mycoplasma pneumoniae have been
associated with antecedent infections.
LABORATORY FEATURES
CSF FINDINGS : Increased CSF proteins (1-10g/dl)
without accompanying pleocytosis.

CSF is often normal when symptoms have been present


for less than 48 hours; by the end of the first week the
level of protein is usually elevated.
DIAGNOSIS
Diagnosis of AIDP is made by recognizing a pattern of
rapidly evolving paralysis with areflexia with with
absence of fever or other or systemic symptoms and
characteristics antecedent events .

DIFFERENTIALS :
ACUTE MYELOPATHIES
DIPHTHERIA
LYME POLYRADICULITIS
TICK BORNE PARALYSIS
VASCULITIC NEUROPATHY
POLIOMYELITIS
TREATMENT
High dose intravenous immunoglobulin
(IVIg) or Plasmapheresis(PLEX) can be
initiated .

IVIg administered as five daily infusions for


a total dose of 2g/Kg bodyweight

A course of PLEX consists of 40-50ml/kg


Plasma exchange (PE) 4-5 times over 7-10
days .
PROGNOSIS AND
RECOVERY
85% of patients with GBS achieve full
functional recovery within several months to
years with minor findings on exmination such
as areflexia which might persist.

Mortality rate is less than5% which usually


occurs due to secondary pulmonary
complications.
THANK
YOU

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